Arterial stiffness is an important physiological parameter because its increase has been associated with a raised risk of cardiovascular disease and stroke. The underlying mechanisms for both conditions, despite the fact that they both increase arterial stiffness, are however different. One is arteriosclerosis, which is the hardening of the arteries as an age-related effect that has a dilatational and weakening effect on the arterial wall, particularly in the aorta and the cerebral arteries. The other is atherosclerosis, which is characterized by the formation of plaques consisting of lipid accumulation, connective tissue fibers and calcium deposits in certain arterial locations and can affect any artery, but frequently attacks the carotid, cerebral, and the iliac arteries as well as certain locations of the abdominal aorta.
The principal components of the arterial walls are elastin and collagen, both of which constitute about 50% of the dry weight, and smooth muscle and non-fibrous matrix. As is the case in most living tissue, about 70% of wet weight is contributed by water. Both elastin and collagen are fibrous materials but the elastic modulus of collagen is significantly larger than that of elastin. The distribution of elastin and collagen is significantly different for the central, and particularly the thoracic aorta, versus the distal aorta and the peripheral arteries. While in the former elastin is the dominant component, representing about 60% of the fibrous material, in the extrathoracic arteries the relative proportion is reversed, with collagen contributing 70%. The enhanced elastic properties of the thoracic artery allow it to act as a Windkessel pressure storage volume during diastole, maintaining pressure in the arterial system when the heart is closed. The less elastic properties of the abdominal aorta and the peripheral arteries cause the propagation velocity of the arterial pressure pulse to increase as it heads into the periphery.
Certain progressive pathological states will change the elastic property, the stiffness, of the arterial tree. Arteriosclerosis, which affects the central and not the peripheral arteries, is generally understood to be the result of the age-related fracture of elastin fibers, the elastic load-bearing elements of the arterial wall. This deterioration causes the wall to weaken and to stretch, with the result that stress is transferred to the collagenous load bearing elements of the arterial wall much earlier in the rising pressure profile of the passing pressure pulse as compared to the case when the elastic elements are intact. The resultant mean increase in stiffness increases the propagation velocity of the arterial pressure pulse, which in turn accelerates the arrival times of the arterial pulse reflections, with deleterious effects. As an example, it is generally accepted that the timing of the iliac reflection is such that it arrives outside the closed heart, i.e. during diastole, so as to generate the static pressure required to force blood into the coronary arteries, which, at right angles to the ascending aorta, require an aortic no-flow high-pressure condition for optimum perfusion. If the reflected pulse arrives earlier, such as while the aortic valve is still open, the heart has to pump against a high pressure peak, an increased stress that can lead to heart disease. The loss in elasticity, particularly of the thoracic aorta, taxes the heart also by reducing or removing the pressure storage capability of that artery during diastole, forcing the heart to work harder. Specifically, complete loss of the pressure storage capability doubles the workload of the heart. This is one of the reasons for the commonly observed increase in pulse pressure with age.
Another pathology that negatively affects arterial stiffness is atherosclerosis, where the arterial elasticity is reduced due to plaque deposits on the artery's interior. Here the particular dangers are ischemia in the tissue downstream of an obstruction that limits or terminates blood flow, localized weakening of the arterial wall with the possibility of aneurysms, and stroke due to deposits being dislocated and traveling to the lung, the brain, or other sites, with potentially catastrophic consequences.
Early detection of an increase in the arterial stiffness and treatment, particularly through lifestyle changes, could consequently help to prevent the serious consequential complications discussed above. A mile marker against which the effectiveness of treatments and progress toward lowering arterial stiffness can be assessed would be beneficial to both clinicians and patients, making screening as well as long-term follow-up more meaningful and more likely to induce adherence to the required lifestyle changes.